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Testicular function in post pubertal male pseudohermaphroditism.

作者信息

Campo S, Stivel M, Nicolau G, Monteagudo C, Rivarola M

出版信息

Clin Endocrinol (Oxf). 1979 Nov;11(5):481-90. doi: 10.1111/j.1365-2265.1979.tb03100.x.

DOI:10.1111/j.1365-2265.1979.tb03100.x
PMID:160294
Abstract

Testicular endocrine function was studied in twelve post pubertal patients with male pseudohermaphroditism and 46 XY chromosomal constitution. Patients were divided into three groups, four subjects who became feminized during puberty, five who became masculinized during puberty and three who were castrated before puberty. Serum dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, androstendione, testosterone, dihydrotestosterone, LH and FSH were determined by radioimmunoassay. Patients of the first group had the clinical characteristics of testicular feminization secondary to absence of the androgen receptor. One of the five patients of the second group had deficient testosterone secretion but no enzymatic defect could be demonstrated. One of the subjects castrated before puberty had a deficiency in 17,20-desmolase. Therefore, evidence of a failure of the fetal testes could be found in only two of the twelve patients studied.

摘要

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A missense mutation in the human cytochrome b5 gene causes 46,XY disorder of sex development due to true isolated 17,20 lyase deficiency.人类细胞色素 b5 基因突变导致 46,XY 性发育障碍,原因是真正的孤立 17,20 裂解酶缺乏。
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